Tải bản đầy đủ (.pdf) (5 trang)

66 the china study the most comprehensive phần 26

Bạn đang xem bản rút gọn của tài liệu. Xem và tải ngay bản đầy đủ của tài liệu tại đây (77.16 KB, 5 trang )

BROKEN HEARTS

113

kink in a garden hose and watering a desperately dry garden with the
resulting trickle of water!
Why hadn't these soldiers had a heart attack already? After all, only
10% of the artery was open. How could that be enough? It turns out
that if the plaque on the inner wall of the artery accumulates slowly,
over several years, blood flow has time to adjust. Think of blood flowing
through your artery as a raging river. If you put a few stones on the sides
of a river every day over a period of years, like plaque accumulating on
the walls of the artery, the water will find another way to get to where it
wants to be. Maybe the river will form several smaller streams over the
stones. Perhaps the river will go under the stones forming tiny tunnels,
or maybe the water will flow through small side streams, taking a new
route altogether. These new tiny passageways around or through the
stones are called "collaterals." The same thing happens in the heart. If
plaque accumulates over a period of several years there will be enough
collateral development that blood can still travel throughout the heart.
However, too much plaque buildup can cause severe blood restriction,
and debilitating chest pain, or angina, can result. But this bUildup only
rarely leads to heart attacks. 9 , 10
So what leads to heart attacks? It turns out that it's the less severe accumulations of plaque, blocking under 50% of the artery, that often cause
heart attacks.ll These accumulations each have a layer of cells, called the
cap, which separates the core of the plaque from the blood flOwing by. In
the dangerous plaques, the cap is weak and thin. Consequently, as blood
rushes by, it can erode the cap until it ruptures. When the cap ruptures,
the core contents of the plaque mix with the blood. The blood then begins
clotting around the site of rupture. The clot grows and can qUickly block
off the entire artery. When the artery becomes blocked over such a short


period of time, there is little chance for collateral blood flow to develop.
When this happens, blood flow downstream of the rupture is severely
reduced and the heart muscles don't get the oxygen they require. At this
point, as heart muscle cells start to die, heart pumping mechanisms begin
to fail, and the person may feel a crushing pain in the chest, or a searing
pain down into an arm and up into the neck and jaw. In short, the victim
starts to die. This is the process behind most of the l.1 million heart attacks that occur in America every year. One out of three people who have
a heart attack will die from it. 9 , 10
We now know that the small to medium accumulation of plaque, the
plaque that blocks less than 50% of the artery, is the most deadly. II , 12


114

THE CHINA STUDY

So how can we predict the timing of heart attacks? Unfortunately, with
existing technologies, we can't. We can't know which plaque will rupture, when, or how severe it might be. What we do know, however, is
our relative risk for having a heart attack. What once was a mysterious
death, which claimed people in their most productive years, has been
"demystified" by science. No study has been more influential than that
of the Framingham Heart Study.

FRAMINGHAM
After World War II, the National Heart Institute l3 was created with a
modest budget4 and a difficult mission. Scientists knew that the greasy
plaques that lined the arteries of diseased hearts were composed of cholesterol, phospholipids and fatty acids, 14 but they didn't know why these
lesions developed, how they developed or exactly how they led to heart
attacks. In the search for answers, the National Heart Institute decided
to follow a population over several years, to keep detailed medical records of everybody in the population and to see who got heart disease

and who didn't. The scientists headed to Framingham, Massachusetts.
Located just outside of Boston, Framingham is steeped in American
history. European settlers first inhabited the land in the seventeenth
century. Over the years the town has had supporting roles in the Revolutionary War, the Salem Witch Trials and the abolition movement.
More recently, in 1948, the town assumed its most famous role. Over
5,000 residents of Framingham, both male and female, agreed to be
poked and prodded by scientists over the years so that we might learn
something about heart disease.
And learn something we did. By watching who got heart disease
and who didn't, and comparing their medical records, the Framingham
Heart Study developed the concept of risk factors such as cholesterol,
blood pressure, phYSical activity, cigarette smoking and obesity. Because
of the Framingham Study, we now know that these risk factors playa
prominent role in the causation of heart disease. Doctors have for years
used a Framingham prediction model to tell who is at high risk for heart
disease and who is not. Over 1,000 scientific papers have been published from this study, and the study continues to this day, having now
studied four generations of Framingham residents.
The shining jewel of the Framingham Study is its findings on blood
cholesterol. In 1961, they convincingly showed a strong correlation between high blood cholesterol and heart disease. Researchers noted that


BROKEN HEARTS

115

men with cholesterol levels "over 244 mgldL (milligrams per deciliter)
have more than three times the incidence of CHD (coronary heart disease) as do those with cholesterol levels less than 210 mgldL."15 The
contentious question of whether blood cholesterol levels could predict
heart disease was laid to rest. Cholesterol levels do make a difference.
In this same paper, high blood pressure was also demonstrated to be an

important risk factor for heart disease.
The importance given to risk factors signaled a conceptual revolution. When this study was started, most doctors believed that heart
disease was an inevitable "wearing down" of the body, and we could do
little about it. Our hearts were like car engines; as we got older, the parts
didn't work as well and sometimes gave out. By demonstrating that we
could see the disease in advance by measuring risk factors, the idea of
preventing heart disease suddenly had validity. Researchers wrote, " . .. it
appears that a preventive program is clearly necessary."15 Simply lower
the risk factors, such as blood cholesterol and blood pressure, and you
lower the risk of heart disease.
In modern-day America cholesterol and blood pressure are household terms. We spend over 30 billion dollars a year on drugs to control
these risk factors and other aspects of cardiovascular disease. 2 Almost
everyone now knows that he or she can work to prevent a heart attack
by keeping his or her risk factors at the right levels. This awareness is
only about fifty years old and due in large measure to the scientists and
subjects of the Framingham Heart Study.

OUTSIDE OUR BORDERS
Framingham is the most well-known heart study ever done, but it is
merely one part of an enormous body of research conducted in this
country over the past sixty years. Early research led to the alarming
conclusion that we have some of the highest rates of heart disease in
the world. One study published in 1959 compared the coronary heart
disease death rates in twenty different countries (Chart 5.1) .16
These studies were examining Westernized societies. If we look at
more traditional societies, we tend to see even more striking disparities
in the incidence of heart disease. The Papua New Guinea Highlanders,
for example, pop up in research quite a bit because heart disease is rare
in their societyY Remember, for example, how low the rate of heart disease was in rural China. American men died from heart disease at a rate
almost seventeen times higher than their Chinese counterparts. IS



THE CHINA STUDY

116

CHART 5.1: HEART DISEASE DEATH RATES FOR MEN AGED 55 TO 59
ACROSS 20 COUNTRIES, CIRCA 1955 16

800I
700I

g
o

I

~

~

600I

I"i


~
~
0..
Q)


fo

SOO
40 0'

+-'

ru

a::
..c 300'

fo

fo

+-'

I"i

ru

Q)

0

200

I"i


100'

o

I
ru
c -0
+-'
ru
ru
.!2
c
+-'
C
Vl
u::: ru
II>
Q)

-0
Q)

.t=

c

:::J

-0


U

.~

~

+-'

II>

::J

«

fh

ru -0 ~ E >- 2- c Q) m c
..:
ru ru ru u c:n..Q
C
c
ru
0
+-'
0.. C
ru ..c ::J
.!2 -0 L.L E -0
II>
>ru ::J Q)

Q)
~ ~ -.
ru .....
U
c:n
::J
ru c:n C C
t
~
Q)
Qj 0
u...
~
U
«
C
0
ru Q)
N
N
co Z
+-'
a...
:>2 E 0 Vl
.~
-0

E -6
Q)


~ -0 ~
Q)
Q)
19
Z .t=

~

c

Q)

Vl

ru
.:;:
ru
Vi
0

c:n
::J

>-

c

:::J

Why were we succumbing to heart disease in the sixties and seventies, when much of the world was relatively unaffected?

Quite simply, it was a case of death by food. The cultures that have
lower heart disease rates eat less saturated fat and animal protein and
more whole grains, fruits and vegetables. In other words, they subsist
mostly on plant foods while we subsist mostly on animal foods.
But might it be that the genetics of one group might just make them
more susceptible to heart disease? We know that this is not the case,
because within a group with the same genetic heritage, a similar relationship between diet and disease is seen. For example, Japanese men
who live in Hawaii or California have a much higher blood cholesterol
level and incidence of coronary heart disease than Japanese men living
in Japan. 19 • 20
The cause is clearly environmental, as most of these people have the
same genetic heritage. Smoking habits are not the cause because men


BROKEN HEARTS

117

in Japan, who were more likely to smoke, still had less coronary heart
disease than the Japanese Americans. 19 The researchers pOinted to diet,
writing that blood cholesterol increased "with dietary intake of saturated fat , animal protein and dietary cholesterol." On the flip side, blood
cholesterol "was negatively associated with complex carbohydrate intake .... "20 In simple terms, animal foods were linked to higher blood
cholesterol; plant foods were linked to lower blood cholesterol.
This research clearly implicated diet as one possible cause of heart
disease. Furthermore, the early results were painting a consistent picture: the more saturated fat and cholesterol (as indicators of animal food
consumption) people eat, the higher their risk for getting heart disease.
And as other cultures have come to eat more like us, they also have
seen their rates of heart disease skyrocket. In more recent times, several
countries have now come to have a higher death rate from heart disease
than America.


RESEARCH AHEAD OF ITS TIME
So now we know what heart disease is and what factors determine our
risk for it, but what do we do once the disease is upon us? When the
Framingham Heart Study was just beginning, there were already doctors who were trying to figure out how to treat heart disease, rather
than just prevent it. In many ways, these investigators were ahead of
their time because their interventions, which were the most innovative,
successful treatment programs at the time, utilized the least advanced
technology available: the knife and fork.
These doctors noticed the ongoing research at the time and made
some common-sense connections. They realized that 2l :
• excess fat and cholesterol consumption caused atherosclerosis (the
hardening of the arteries and the accumulation of plaque) in experimental animals
• eating cholesterol in food caused a rise in cholesterol in the blood
• high blood cholesterol might predict andlor cause heart disease
• most of the world's population didn't have heart disease, and these
heart disease-free cultures had radically different dietary patterns,
consuming less fat and cholesterol
So they decided to try to alter heart disease in their patients by having
them eat less fat and cholesterol.
One of the most progressive doctors was Dr. Lester Morrison of Los



×